Quid faciam de resistentia medicamentorum non parvae cellae pulmonis pulmonis iaculis medicinae, hic scire vis
Lung cancer is the cancer with the highest morbidity and mortality in China. About 1.6 million people die of this disease each year worldwide, and about 85% of these cases are non-small cell lung cancer (NSCLC). At present, many cancer-targeting drugs have been developed for advanced cellula parva non-pulmonis cancer in the world. These new therapeutic drugs have increased the median survival time of patients to 35 months, which not only significantly prolonged their life span, but also achieved Personalized treatment. However, most patients will develop secondary drug resistance 8 to 14 months after receiving EGFR-TKI (standard first-line treatment for patients with sensitive mutations in the EGFR gene). How to solve the problem of drug resistance has become a hot research topic. Will continue to answer for everyone.
1. Cur enim non-Lorem targeted parva cellula pulmonis cancer obsistens?
Mauris iaculis resistentia primae et secundae in certamine solet movere.
1. Prima medicamento resistentia immunibus: patientes estote ad proprium scopum mutationes EGFR refers, sed ex natura coram KRAS gene mutationes, et gefitinib erlotinib dose medicinae targeted aliis tabulis, quae non effective, III post mensibus usus medicamento resistentia occurs.
2. secundarium medicamento resistentia immunibus: In the course of targeted drug treatment, because the target signal pathway continues to be inhibited by drugs, the tuberculum produces other gene mutations in order to escape the drug, inhibiting the therapeutic effect of the targeted drug on the EGFR target, thereby Lead to drug resistance. The effective time of medication is usually more than 3 months.
2. Lorem targeted pro non-medicamento resistentia mechanism est parva cellula pulmonis cancer
There are currently three specific mechanisms for non-small cell pulmonis cancer, drug resistance. First, drug resistance is generated through genetic mutation. About 40% of the genes in patients with positive genetic tests will generate new genes from the original genes, which will cause insensitivity to the original drugs, resulting in drug resistance. Secondly, the cunning cancer cells will usually “repair the dark path of the plank road” and take a detour. This situation accounts for about 20% of patients with drug resistance. In addition to the above two drug resistance pathways, the drug resistance mechanism of the remaining 30% of patients is not yet clear.
3. Quomodo si judicas aegris cum non-medicamento resistentia est parva cellula pulmonis cancer?
1. Plerumque, medicamento renitente, medicamentum iaculis non potest continere incrementum tumoris, qui tumorem augere vel metastasizare longe faciet. Hoc tempore aeger quaedam signa habebit, qualia non prius tussis, sed recens tussis, vel post metastasim cerebri aegrum vertigine, capitis, vomitu sine causa, et patienti metastasin ossis dolorem experietur, compressionem nervi et nervum. alia eaque. Hoc tempore aeger vigilare debet.
2. Nam, ut aegris qui develop medicamento resistentia, cum sit optimus via ut ire pro ordinarius review hospitium. Ad determinare utrum resistat per tumorem medicamento targeted venalicium et imagine examen.
4. Postquam develops patientes estote ad medicamento resistentia, alter medicus plerumque suadeo biopsy, quid sibi vult
Et generaliter omnes aegris cum morbo pulmonis cancer, qui ut habeat medicamentis uti Tri-EGFR progressum patibulum subire volulstri alter biopsy.
1. Serena vitiatam esse naturam acutius iterum ad determinare si est non cancer cancer a primaria coetus.
2. Secundum geneticae probationis exsequere num medicamento resistentiae ex mutatione gene iterum causata sit et deprehendas num novum consilium curatio iaculis sit.
Secunda biopsy statim progressum morborum deprehendere potest, mechanismos medicamentorum resistentiae revelare et opportuna consilia curatio curationi sequi. Secunda biopsy maxime dividitur in corpus biopsy et liquidum biopsy. TEXTUS biopsy praecipue dividitur in biopsy thoracotomia, biopsy bronchoscopia, et pulmonis percutaneous biopsy. Aegris, qui tumorem textus obtinere non possunt, liquida biopsy secundum sanguinem NGS gene technologiae sequelae technologiae eligi possunt ad ulteriores curationes occasiones obtinendas.
5. Quid faciam, si medicamento resistentia, postquam comparuerit primo-generationem de non-Lorem TKI targeted parva cellula pulmonis cancer?
Primum genus, EGFR TKI includit gefitinib, erlotinib et icotinib.
Secundum NCCN guidelines, T790M mutationem probatio sumitur primum suadetur, cum primum generatio EGFR TKI bellum. An non habet patientes estote ad diversa se raptantes, adoptati sunt signa, sive sit cerebrum metastasis vel plures progressum et progressum loci.
1. Pro patientibus positivum T790M et Prima commendatio est curatio Osimertinib, curatio TKI pro aegris lento progressione continua, et curatio localis aegris cum progressione locali, inclusa radiotherapia metastasis cerebri, radiotherapia localis unius vitii Ut chemotherapy pro patientibus magno progressu capiat.
2. T790M, negans enim aegris, chemotherapy detur vel immunotherapy may be selected based on the PD-L1 expression of the patient.
3. Nam cum aegris qui asymptomatic medicamento resistentia immunibus: loci curatio potest et sublatus est generationem continued TKI curatio. Cum aegris cerebrum nisi metastases, loci curatio potest considerari et permanere uti in prima generatione, EGFR TKI.
6. longum et develop a captis propioribus osimertinib medicamento resistentia?
Osimertinib est tertia generatione EGFR TKI targeted medicamento-average cum medicamento resistentia periodum circiter XI menses. Sed orci applications, et multis aegris cum duo vel tres annos post captivitatis osimertinib develop resistere ictu mutationes, ita tempus est propria rei de oxitinib resistente variatur a persona ad personam.
7. Quid est mechanism de medicamento resistentia osimertinib?
Et medicamento resistentia mechanism de osimertinib est valde interdum eget, inter C797S mutationem, MET extollendam / MEIO novam commixtionem / ros-I novam commixtionem, NEC-II existimavit, BRAF mutationem, RAS mutationem, FGFR1 mutationem, conversionem ad parva cellula pulmonis cancer, ibi sunt geneticae mutationes, et cetera, et dein diaetam ipsis constituam pro medicamento praevalentes machinationes diversis in diversis medicamento resistentia.
1. EGFR gene mutationes iterum: EGFR796 DCCXCVII mutationes et reputatus 797%, reputatus 24.7% EGFR DCCXCII mutationes, mutationes DCCXIX EGFR DCCXVIII, et ille reputatus 792% -EGFR gene, re-repugnant mutationum, unde omnis XLV% de aegris, ad dimidium prope est.
2. Alius gene mutationes; inter PIK3CA, BRAF, MET, rei, KRAS, etc. A common et varietate genes rarum pulmone cancer sunt implicari, et coegi sunt rariores.
3. Transfiguratus in cell parva pulmonis cancer.
8. Quid est Lorem post Oxitinib targeted ad medicamento resistentia?
Alia enim resistentiae genes, ut initialis solutio si ponatur, sequitur,
1. Triplex enim est causa per mutationem (C797S / T790M / del-XIX), cum effectus melius est illic eligendorum bugatinib osimertinib / gefitinib, affectus et effectus, non autem per spatium locale C19S et T797M. (I) Bugatinib EGFR combined per anti-genus (cetuximab / panitumumab) potest augendae effectus therapeutici, tergemini nece mutationes, et simul duo medicinae potest ludere a synergistic effectus; (II) Bugatinib combined per Selumetinib (Simetinib) potest vincere posse resistentiam osimertinib C790S fecit per mutationem.
2. Ordinatio EGFR C797S Nam trans-Ac primum, cum tertia generatione targeted generation targeted medicinae medicinae, ut combined per osimertinib gefitinib / erlotinib. Nam Cis-alignment, vos can
elige + Bugatinib VEGF targeted medicaménta utíliter.
3. Si solus est C79CS mutationem, vos can utor a prima-generationem EGFR inhibitor, ut gefitinib, erlotinib, icotinib.
4. MET insinuat, quod illa, tum amplificata osimertinib combined per MET inhibitors (camatinib, crizotinib, Savolitinib, etc.). Suadeant ut combined per mutationes BRAF osimertinib BRAF inhibitors (+ dalafinib trametinib). Ret, ut suggesserant Osimertinib combined per mutationem Kabotinib et utique melior sit Osimertinib combined per GRN-DCLXVII.
Factum est autem post oxetinib repugnantia suadetur, optimum est facere per geneticae test item, quod lego appropriate targeted medicamento secundum mutationem meliorem ad scopum auxilium curatio. Est optimum medicus est consiliamini professionalis targeted ad compositum justo a mauris.
9. Parte effectus non parva cellula-pulmonis cancer medicinae targeted
In scopum hypotheticarum targeted medicinae patet, qui vult, sed quia non orci non adversa reactiones Dominus fieri. Et adversa reactiones de targeted sicut fluxus medicinae, proteinuria, altum sanguinem pressura, cor morbo acne-ut oboedienter exequendum bene nota sunt. Etsi minus quam traditional Cytotoxic targeted medicinae medicamento, tamen ut non sint minoris. Quidam rara adversa reactiones sunt saepe diffice est egritudo, quod est orci diagnosis, saepe ducens ad momenta rerum pendent.
Eg erlotinib curatio potest facere asymptomatic iecoris transaminase elevation: et gastrointestinal cruenti quod raro retulit, dum gefitinib est parva moleculo anti-EGFR targeted Lorem, quamquam sua metabolismi est maxime iecoris circiter IV% exeant qui e renibus in forma prototypes et tenuissimum, et amet prone ut acuti renum defectum, medicamento quod amplio post receptum angustias progressos. In Lorem targeted medicamento, gravibus et adversa reactiones letalis ipsa fugienda esse concedant quod possibile est. Adversa reactiones et voluntas afficit enim patientes fiducia est apud curatio. Gravis adversa reactiones treatment processus potest impediri.
